isoproterenol - CAS 7683-59-2
Catalog number: 7683-59-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C11H17NO3
Molecular Weight:
211.26
COA:
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Targets:
Adrenergic Receptor
Description:
Isoproterenol can be used for the treatment of bradycardia (slow heart rate), heart block, and rarely for asthma. It is a non-selective β adrenoreceptor agonist and TAAR1 agonist that is structurally similar to epinephrine.
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Purity:
98%
Appearance:
Powder
Synonyms:
Isoprenaline; Norisodrine; Novodrin; Isoprenalin; Asiprenol;4-[1-hydroxy-2-(propan-2-ylamino)ethyl]benzene-1,2-diol;51-30-9(hydrochloride)
Solubility:
Soluble in DMSO
Storage:
-20℃ Freezer
MSDS:
Inquire
Application:
bradycardia (slow heart rate), heart block, and rarely for asthma.
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Quantity:
Milligrams-Grams
Melting Point:
165 - 170℃
InChIKey:
JWZZKOKVBUJMES-UHFFFAOYSA-N
InChI:
InChI=1S/C11H17NO3/c1-7(2)12-6-11(15)8-3-4-9(13)10(14)5-8/h3-5,7,11-15H,6H2,1-2H3
Canonical SMILES:
CC(C)NCC(C1=CC(=C(C=C1)O)O)O
1.Downregulation of β-Adrenoceptors in Isoproterenol-Induced Cardiac Remodeling through HuR.
Yin Q1,2, Yang C2, Wu J2, Lu H2,3, Zheng X3, Zhang Y2, Lv Z2, Zheng X1, Li Z2,4. PLoS One. 2016 Apr 1;11(4):e0152005. doi: 10.1371/journal.pone.0152005. eCollection 2016.
β-adrenergic receptors (β-ARs) play an important role in cardiac remodeling, which is the key pathological process in various heart diseases and leads to heart failure. However, the regulation of β-AR expression in remodeling hearts is still unclear. This study aims to clarify the possible mechanisms underlying the regulation of β1- and β2-AR expression in cardiac remodeling. The rat model of cardiac remodeling was established by subcutaneous injection of isoproterenol(ISO) at the dose of 0.25 mg·kg-1·d-1 for 7days. We found that the expression of β1- and β2-ARs decreased in the remodeling heart. The mechanisms may include the inhibition of DNA transcription and the increase of mRNA degradation. cAMP-response element binding protein(CREB) is a well-known transcription factor of β-AR. However, the expression and activation of CREB was not changed in the remodeling heart. Further, human Antigen-R (HuR), a RNA binding protein, which binds to the 3'-untranslated region of the β-AR mRNA and promotes RNA degradation, was increased in the remodeling model.
2.Endoplasmic Reticulum Stress is Involved in DFMO Attenuating Isoproterenol-Induced Cardiac Hypertrophy in Rats.
Lin Y, Zhang X, Xiao W, Li B, Wang J, Jin L, Lian J, Zhou L, Liu J. Cell Physiol Biochem. 2016 Apr 14;38(4):1553-1562. [Epub ahead of print]
BACKGROUND/AIMS: Studies performed in experimental animals have shown that polyamines contribute to several physiological and pathological processes, including cardiac hypertrophy. This involves an increase in ornithine decarboxylase (ODC) activity and intracellular polyamines associated with regulation of gene expression. Difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, has attracted considerable interest for its antiproliferative role, which it exerts through inhibition of the polyamine pathway and cell turnover. Whether DFMO attenuates cardiac hypertrophy through endoplasmic reticulum stress (ERS) is unclear.
3.Decreased Polycystin 2 Levels Result in Non-Renal Cardiac Dysfunction with Aging.
Kuo IY1, Duong SL1, Nguyen L1, Ehrlich BE1,2. PLoS One. 2016 Apr 15;11(4):e0153632. doi: 10.1371/journal.pone.0153632.
Mutations in the gene for polycystin 2 (Pkd2) lead to polycystic kidney disease, however the main cause of mortality in humans is cardiac related. We previously showed that 5 month old Pkd2+/- mice have altered calcium-contractile activity in cardiomyocytes, but have preserved cardiac function. Here, we examined 1 and 9 month old Pkd2+/- mice to determine if decreased amounts of functional polycystin 2 leads to impaired cardiac function with aging. We observed changes in calcium handling proteins in 1 month old Pkd2+/- mice, and these changes were exacerbated in 9 month old Pkd2+/- mice. Anatomically, the 9 month old Pkd2+/- mice had thinner left ventricular walls, consistent with dilated cardiomyopathy, and the left ventricular ejection fraction was decreased. Intriguingly, in response to acute isoproterenol stimulation to examine β-adrenergic responses, the 9 month old Pkd2+/- mice exhibited a stronger contractile response, which also coincided with preserved localization of the β2 adrenergic receptor.
4.Safety pharmacology studies using EFP and impedance.
Obergrussberger A1, Juhasz K2, Thomas U2, Stölzle-Feix S2, Becker N2, Dörr L2, Beckler M2, Bot C2, George M2, Fertig N2. J Pharmacol Toxicol Methods. 2016 Apr 12. pii: S1056-8719(16)30033-8. doi: 10.1016/j.vascn.2016.04.006. [Epub ahead of print]
INTRODUCTION: While extracellular field potential (EFP) recordings using multi-electrode arrays (MEAs) are a well-established technique for monitoring changes in cardiac and neuronal function, impedance is a relatively unexploited technology. The combination of EFP, impedance and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) has important implications for safety pharmacology as functional information about contraction and field potentials can be gleaned from human cardiomyocytes in a beating monolayer. The main objectives of this study were to demonstrate, using a range of different compounds, that drug effects on contraction and electrophysiology can be detected using a beating monolayer of hiPSC-CMs on the CardioExcyte 96.
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CAS 7683-59-2 isoproterenol

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